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Akira Yamauchi, Izumi Takei, Akira Kasuga, Yuko Kitamura, Norimi Ohashi, Satomi Nakano, Sumiyo Takayama, Shinya Nakamoto, Fuminori Katsukawa and Takao Saruta

Yamauchi A, Takei I, Kasuga A, Kitamura Y, Ohashi N, Nakano S, Takayama S, Nakamoto S, Katsukawa F, Saruta T. Depression of dehydroepiandrosterone in Japanese diabetic men—comparison between non-insulin-dependent diabetes mellitus and impaired glucose tolerance. Eur J Endocrinol 1996;135:101–4. ISSN 0804–4643

Hyperglycemia is known to reduce dehydroepiandrosterone (DHEA) circulating levels; however, the mechanism by which hyperglycemia decreases DHEA is not elucidated. In this study, serum DHEA and DHEA sulfate (DHEA-S) levels were compared in 50 men with non-insulin-dependent diabetes mellitus (NIDDM) and 50 age-matched men with impaired glucose tolerance (IGT) receiving only diet therapy. Serum concentrations of DHEA and DHEA-S in the NIDDM group were significantly lower than in the IGT group (7.8 and 9.7 nmol/l vs 3.4 and 4.9 μ mol/l, respectively; p< 0.01) but there was no significant difference in immunoreactive insulin between the two groups. When the results from both groups were combined, HbA1c was significantly inversely related to DHEA (r = −0.243. p<0.01) and DHEA-S (r = −0.305, p<0.01). Immunoreactive insulin showed no correlation with DHEA and DHEA-S. Multiple regression analysis showed that HbA1c was independently negatively related to both DHEA and DHEA-S. We conclude that hyperglycemia may decrease serum DHEA and DHEA-S in Japanese men with NIDDM, but the depression of DHEA(-S) is independent of serum insulin level.

Akira Yamauchi, Department of Internal Medicine, Keio University School of Medicine. 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan

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Akira Sugenoya, Emiko Mizuno, Masayuki Haniuda, Minoru Fujimori, Hiroyuki Masuda, Yoshio Kasuga, Shinya Kobayashi and Futoshi Iida

Abstract.

The presence of thyroid hormone autoantibodies was investigated in a 48-year-old non-goitrous woman with high levels of serum total T3 and free T3. Her other thyroid function tests were normal. The presence of thyroid hormone autoantibodies were assessed in serum, acid-charcoal treated serum, IgG fractions and in a purified IgG fraction. The IgG fraction was separated from serum by a protein A-Sepharose CL-4B column chromatography and purified by gel filtration chromatography using Sephacryl S 200. Sera from normal individuals were used as controls. The results showed that the increased serum total and free T3 levels were caused by the presence of anti-T3 IgG autoantibodies. The results also indicate that protein A column chromatography is useful as a screening method for gross qualitative analyses of thyroid hormone autoantibodies.

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Akira Sugenoya, Shinya Kobayashi, Yoshio Kasuga, Hiroyuki Masuda, Minoru Fujimori, Makoto Komatsu, Shozo Takahashi, Shiro Yokoyama, Tadahiro Shimizu, Takashi Yamada and Futoshi Iida

To clarify the intrathyroidal accumulation of TSH receptor antibody (TR-ab) produced in the thyroid, adrenalin was injected directly into the thyroid artery of patients with Graves' disease during surgery, allowing serial determination of the TR-ab levels in the thyroidal venous blood. Nine surgical patients (3M and 6F) with Graves' disease and receiving anti-thyroid drugs preoperatively for a period of one to four years were enrolled in this study. Comparison between pre- and post-treatment TR-ab levels revealed continuous increments from the pretreatment levels within 15 min of the injection in five (55.6%) of the nine patients. In three of the five patients, TR-ab levels that had been negative before adrenalin injection became positive 1 min after injection. It is assumed that the increase in the TR-ab level is due to adrenalin-induced constriction of the capillaries in the thyroid tissues, resulting in a voluminous flow of the TR-ab retained in the thyroid into the vein. These findings indicate that the TR-ab level in the peripheral blood does not necessarily reflect precisely the abnormal immunological condition in the Graves' thyroid.